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DISOR DER S OF LA UG HTER DU E TO BRA IN LESIONS 1BY

REDVERS IRONSIDE{Maida Vale Hospital, London, W.9)W E know very little abo ut the physiology of no rm al laughter. W e arestill ignorant of how facial expressions in smiling are mediated, whetherby cortical or subcortical structures. Cortical and m id-brain tracts con-nected with the nervous control of respiration and probably importantin laughter, are known to exist, but their relationship to emotional ex-pression is disputab le. The neurological mechanisms underlying theem otional states of mirth or joy which usually accomp any n atura l laughterare even less und erstoo d. Philosophers, psychologists and neurologistshave tried to explain in the language of their individual disciplines howwe come to " see a joke " or make a witty remark.Recent discoveries relating to the anatomy and physiology of the

thalamus, hypothalamus, their cortical connexions and their relationshipswith the limbic structures of the temporal lobe, suggest that a review ofthe facts concerning disordered laughter resulting from focal cerebrallesions may not be inopportune.Disordered laughter (or disordered weeping) from brain damage is aclinical curiosity except in cases of pseudo-bulbar palsy due to cerebralvascular disease, or certain cases of adva nced mu ltiple sclerosis. In suchcases we usually find during life bilateral extensor plantar responses, andat autopsy evidences of bilateral degeneration of cortico-hypothalamicand cortico-bu lbar tracts. Disordered laugh ter, however, also occurs withdiscrete single brain lesions. This has been less generally recognized. Incertain rare cases of epilepsy disordered laughter may occur during partof the fit. In gross lesions involving fronto-hy poth alam ic conn exions thedisordered laughter appears to be the result of an excited emotional state.

NORMAL LAUGHTER AND SMILINGNatural laughter may be considered as consisting of two components:(1) the more voluntary phenomena of facial expression in smiling, and(2) the more automatic laryngeal and respiratory phenomena in laughing.Expressed in an othe r w ay we may say that the emo tional expression whichlPresidential Address, Neurological Section, Royal Society of Medicine, London;read October 6, 1955.

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5 9 0 REDVERS IRONSIDEwe call laughter consists of facial movements and a respiratory state inwhich rhythm ic clonic expirations produce phon ation . This impliesactivity of bo th som atic and a utono mic functions. N o t only is respira-tion (normally under chemical control) altered in rhythm, but theremay be rise of pulse-rate, flushing and evidences of the outpourings ofinternal and external secretions.The subjective emotional state of which laughter is the expressionis usually, bu t not invariably, one of amusem ent or joy . The stimulusarousing the amusement may proceed from our thoughts, but more com-monly it comes through visual, auditory, cutaneous (tickling), or otherafferent pathw ays. Th e laughter response is pro por tiona l to the stimulus indegree and duration, and to the feeling of amusement which accompaniesthe act.

It is difficult to explain the existence of human smiling and laughterwith their autonomic accompaniments unless they have to do with anecessity in m an to com mu nicate his feelings to other s. An ima ls showtheir emotions or reactions to a situation by noises or gestures inad equ atefor us. In m an , expressive and em otional movem ents of the face, as insmiling, act more or less automatically as gestures of speech, reinforcing,giving emphasis, vividness and energy to conversation, quickening atten-tion and sympathy and conveying shades of meaning not otherwiseexpressed.In conversational speech, alterations in tonus of the laryngeal mus-culatu re togeth er with respira tory adjustm ents give rise to vocal inflections.Such emotional sounds, expressed whether with or independently oflangua ge, signify reactions to our intern al em otion al state. They occu rin animated propositional speech, and in emotional interjections.The bulbar automatisms of laughter are respiratory phenomena adaptedto th e display of em otional feeling. Th e fact tha t they are n orm allyinduced by a pleasant emotion gives them a neurological status higherthan that of other respiratory automatisms, such as coughing, hiccoughand chok ing. Yaw ning is prob ably in an intermediate position havingregard to its association with boredo m. In the Jacksonian sense thebulbar automatisms of laughter seem to be represented at the highestlevel as well as at the lowest.

DEFINITIONS OF PATHOLOGICAL LAUGHTERThe laughter which we meet in focal cerebral disease never resemblesna tur al laug hter. Eithe r the sou nd s or facial expressions are intrinsicallydifferent, or else the em otion behind the laughter is abse nt, or so d isorderedas to render the sounds inappropriate, contradictory or purposeless.This study is largely confined to disorders of the emotional expression

of laughter. The term "pathological laughter"' is usually restricted toconditions where the facio-respiratory mechanism is out of control as

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DISORDERS OF LAUGHTER 5 9 1the result of focal b rain disease or epilepsy. In this cond ition inv olun taryspasmodic attacks, superficially resembling the motor manifestations ofna tura l laughter, occur witho ut app rop riate emotional feeling. Suchattacks are uncontrollable and prolonged and may change from laughterto weeping. Disordered laughter, however, ma y arise when hy poth alam icas well as bulbar mechanisms are acting involuntarily.In emotional liability or emotional incontinence the patient gives onethe impression at first sight that he is the subject of an ever-alteringaffective state which is continually playing upon his laughter mechanism.This may be so, but in most cases these manifestations seem to theobserver to be unaccompanied by those changes in emotional feelingwh ich the pa tient seems to express. Patie nts have great difficulty inm akin g introspective analyses of their laughter-spells. M ost pseu do-bu lbar cases will adm it tha t it is mirthless. Others seem to feel am usem entin some degree as the laughter-spell develops.The exaggeration of the motor responses of excessive laughter callsto mind Henry Head's description of the exaggeration and persistenceof the sensory response in lesions of the thalamus: "It is as if a sparkfired the magazine and the consequences were not commensurate with thecause ."Two other adjectives are sometimes applied to pathological laughter"ina pp rop riate", "con tradicto ry." These imply some alteration eitherpositive or negative in the emotion itself; but not necessarily so, for thenormal feeling may be there whilst the patient is incapable of expressingit except by sounds resembling those of unc ontrollable laughter. Am ong stthe criteria of pathological laughter I would place high the labihty of theresponsehow it may change to sobbing or wailing even in the middleof a burst tha t began as laugh ter. In the m ore exaggerated reactions itmay be exceedingly difficult to tell from the expression on the patient'sface whether he is laughing or weeping. Th e upper par t of the face ma yseem to express anguish or woe an d the lower pa rt laughter. In theslighter reactions there is usually no do ub t as to th e type of facial resp onse.

NEUROLOGICAL SURVEYS AND THEORIESThe earliest clinical studies were those of Oppenheim and Siemerling(1886), Nothnagel (1889) and Brissaud (1895). In 1912 Charles K. Millswrote on "The Cerebral Mechanism of Emotional Expression."S. A. Kinnier W ilson's paper (1924) on "Pathological Laugh ing an dCry ing" is probab ly the one which m ost of us here would ta ke as a basisof approa ch to this subject. Kinnier W ilson pointed out that pa thologicallaughter and crying are allowed by 4lesions of the voluntary paths of them oto r cortex, or by any state in which they exert imperfect con trol. H epostulated a centre linkihg the seventh nerve nucleus in the pons with themotor nucleus of the tenth^nucleus ambiguus) in the medulla, and theBRAIN V OL. LXXDC 3 9

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5 9 2 REDVERS IRON SIDEphrenic nuclei in the upper cervical cord. "By all analogies," he w rote,"this centre must be supranuclear: for the sake of argument we maysuppose it has an upp er pontine site." This hypothetical facio-respiratory"centre" was, he considered, under double control: (1) voluntary throughthe cortico-bulbar part of the pyramidal tract, and (2) involuntary throughtwo of the four respiratory tracts which W alter Spencer (1894) haddem onstrated in mon key s' brains on the basis of stimulation experiments.These tracts w ere said to arise in the posterior orb ital gyrus and to descendto the bulb, converging near the mid-line in the subthalamic region andtegm entum . They had both accelerator and depressor functions and thusfitted into W ilson's theory very neatly, for he could in this way explainthe mainly expiratory character of laughter and the mainly inspiratorycharacter of weeping.

Charles Davison and Harold Kelman (1939) in their paper "Patho-logic Laughing and Crying" dealt not only with the disorders of laughterpathw ays, bu t also with their attend ant em otional disorders. M any oftheir cases were single lesions. F ro m a series of 53 cases with 33 autopsies(6 tumours) they concluded that the hypothalamic or some other of thediencephalic nuclei under cortical control were the main centres for therelease of affective responses. They considered th at th e thalam ic nuclei,striatum and pallidum might also act as centres for the production ofaffective respon ses. Possibly separate pathw ays o r centres existed inintimate connexion with the hypothalamus and the facio-respiratorynuclei in the mesencephalon and metencephalon.I think that Foerster and Gagel (1933) were amongst the first neuro-surgeons to stress the importance of the hypothalamus in the productionof states of excitement with laughter and manic speech; although statesof excitement and apathy in hypothalamic tumours had been observedpreviously by Cushing (1912) and by Fulton and Bailey (1929).Purdon Martin (1950) wrote on "Fits of Laughter (Sham Mirth) inOrganic Cerebral Disease." He considered that the evidence adducedfrom personal and other cases gave practical support to the view that a

motor "centre" for laughter is situated in or near the hypothalamus.He emphasized that the "centre" which discharges in these cases was amotor centre and not one exciting emotion.I shall describe various clinical manifestations of disordered laughter.I propose to show that focal lesions in widespread areas of the brain cancause disturbanc es of emotion an d of laugh ter at different levels. Fo callesions in the pre-frontal an d frontal, tem pora l and limbic lobes may causedisturbances of laughter, particularly if they lie near the mid-line in theneigh bourh ood of the hypothalam us and third ventricle. Involvement ofboth hemispheres or cortical tracts converging towards the mid-line isusu al, but no t inva riable. I shall discuss laugh ter as an epileptic sym ptomand its relationship to temporal lobe epilepsy.

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DISORDERS OF LAUGHTER 5 9 3MATERIAL

In order that the localizing value of the lesion or lesions might beassessed, cases du e to single lesions were soug ht. Th e clinical recordsof 20 cases of uncomplicated bulbar palsy due to motor neurone disease,where the lesions are believed to be confined tothe motor system (onewith autopsy ) were studied . Th e single lesions were tu m ou r cases withautop sy from the literature, and two person al cases with autopsy. Per-sonally observed cases of epilepsy, where the fits appeared as bouts oflaughter are quoted and one personally observed case of prolongedlaughter cu lminating in hemiplegia. It is up on th e study of isolated focallesions that this paper is chiefly based, e.g. tumours, aneurysms.

It is to be emphasized that disorders of laughter are more commonlydue to diffuse lesions such as a rteriosclerosis, multiple sclerosis, encephalitis(lethargic, syphilitic), dystonia musculorum, hepato-lenticular degenera-tion and severe, diffuse head injury; but as these diffuse lesions are of littlelocalizing value attention has been pa id to rarer m ore discrete lesions.

CLINICAL MANIFESTATIONS OF DISORDERED LAUGHTERThe clinical classification of laughter disorders is fraught with dangersand difficulties. A utom atic bulba r sounds of laughter may arou se in thepa tien t some em otio nal feeling as a secondary ma nifestation. This feel-ing is sometimes emba rrassment; i t may, however, be amusem ent. W hen

the appropriate emotional feeling should be anger or grief, the patientlaugh s. In m any cases emotional feeling is abse nt durin g these spells.Spells of prolonged laughter lasting hours or days may occur culminatingin hemiplegia, stupo r or dementia. Fits of laughter may occur as anepileptic phenomenon.It is difficult to make a clear line of distinction between such cases anddisorders of laughter which arise as the result of emotional excitement(e.g. eup ho ria) or from loss of volitional contro l (e.g. confusion, dem entia).In this connexion we may recall the observation of Gowers regardingnatu ral laughter. "T he will is need ed," he said, "n ot to effect it, but torestrain it."I shall describe (1) Invo luntary and explosive laughter in pseud o-bulbarand bulbar syndromes; (2) Fits of laughter as an epileptic phenomenon(including "ictus ridenti"); (3) Disorders of laughter consequent uponexcitement, euphoria and other mental changes.Disorders of smiling demand separate consideration.(1) Involuntary and Explosive Laughter in Pseudo-bulbar and BulbarSyndromesIn the spastic explosive laughter of pseu do-b ulbar an d bulb ar palsy

the facial and the bulbar muscles have imposed upon them the effectsof spasticity, rigidity or paralysis. Th e facial expression in laug hterwaxes an d wanes slowly. A sudden explosion of laughter m ay persist

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5 9 4 REDVERS IRONSIDElike a sustained clonus, and the noise made may be prolonged and dis-torted to a scream or a wail. The sound and appearance resembles thatof a laughing or weeping infant. Sialorrhoea and dysphagia with chokingare common, and the jaw-jerk is increased. Disorder of conjugate ocularmovement on upw ard,. downward or on lateral gaze, or bilateral lidretraction may accompany these phenomena. Evidences of bilateralpyramidal disease are usually, but not invariably, present. This conditionis known to all of you and I propose to describe only one arterioscleroticcase.Bulbar symptoms may result from symmetrical cortical lesions as in thefollowing case (Friedman, 1939):

Autopsy showed almost symmetrical softenings of the lower portions of both motorareas low dow n."Th e patient presented signs of almost complete bulbar paralysis. Th e tongue laylimp in the floor of the m outh. She was unable to swallow or to show her teeth. Shewas, however, subject to sudden outbursts of uncontrolled laughter, so that the wardwas in a constant u pro ar. Du ring these spells emotional o r mim etic movem ents ofthe facial muscles functioned excessively."This case demonstrated in almost experimental fashion the dissociation betweenvoluntary innervation of the facial muscles and the involuntary innervation, which issupplied by way of the so-called facio-respiratory pathw ay. Th e voluntary pathw aywas seemingly damaged on b oth sides and therefore released the involuntary pathway swith resulting gales of laughter."

In pseudo-bulbar cases softenings are found in the corpus striatum,brain-stem and pons. Lesions in the cortex are rare (Hughes, Dodgsonand Maclennan, 1954). In cases with dementia brain shrinkage may bepresent.There are few instances recorded with autopsy findings where patho-logical hilarity followed a single ictus. The lesion in these cases seemsto be a partial occlusion of the vertebral or basilar arteries, producing areasof softening in the m id-line structures of the upper pons or crura cerebri.Thus in C. K. Mills' Case 2 (1912) the lesion involved the red nucleus onthe right side and extended across the mid-line to the left cms.I have not been able to convince myself that pathological laughterhas any close association with thalamic hemiplegia. In W ilson's (1924)Case 5 there was no autopsy and the lesions may well have been multiple,and in W eisenburg and Guilfoyle's (1910) tumour case the autopsy showeddistortion of the hypothalamus.Since it has been denied that pathological laughter occurs in bulbardisease, I considered that the study of motor neurone disease might be ofimportance. W e know tha t the lesions are confined to the motor nucleiand tracts.I studied the case histories of 20 cases of uncomplicated bulbar palsy

due to motor neurone disease, discarding all cases with hypertension,gross memory defects or dementia, and those with reactive depression.

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DISORDERS OF LAUGHTER 5 9 5The difficulties of distinguishing between the crude bulbar automatismsof mirthless laughter and emotional lability is seen in this group of cases.Of 12 cases with extensor responses (2 unilateral only), 5 cases haddisorders of emotional expression described as "poor emotional control,""uncontrollable laughter," "inappropriate laughter," "incongruity ofaffect (grinned when scolding the children )," "em otiona l we eping." Th eothers showed norm al responses. Of 8 cases with flexor responses, 3 haddisorders of emotional expression described as "explosive laughter,""em otionally labile (2)." One had an attack of laughing and screaminglasting three hou rs althou gh n ot a hysterical personality. Th e othersshowed no rma l emotional responses. On e has to explain why in the caseswith bilateral extensor responses, 7 had no abnormal emotional display.Presumably sufficient cortico-bulbar fibres remained to exert controlover the facio-respiratory nuclei. Th ree of the cases with no clinicalevidences of pyram idal disease had d isorders of laughter. Th e dischargeof laughter is in terms of movements, not muscles. The degenerationof bulb ar nuclei-seems to cause disorder of suprasegmental m echanism s.

Case 1.Atrophic bulbar palsy due to uncomplicated motor neurone disease with boutsof laughing or weeping in the early stages of the illness. Plantars flexo r right and left.W. S., aged 47 years, had for eight months complained of inability to formulatewords, a sensation of a lump in the th roa t, difficulty in swallowing, with twitchings inthe arm muscles. Normally she was a stable person emotionally, bu t in the earlymonths of her illness she had irresistible outbursts of weeping or laughter.On examination, she was not particularly depressed, memory and concentrationwere good and her men tal state appeared norm al. The fundi, pupils and externalocular movements were normal. The jaw-jerk was very brisk. There was slight weak-ness of the orbiculares oculi muscles, the palate moved poorly, the tongue was wastedand showed marked fasdculation. The upper limbs showed a loss of power in theright triceps and slight weakness of both wrists and small muscles of the hands.The forearm and han d muscles were wasted a nd there was occasional fasdculation inthe muscles of the shoulder girdles, arm s, forearms and dorsal interossei. The to nuswas flacdd. The trunk and lower limbs, however, were unaffected. Th e tendon re -flexes showed diminution of the triceps-jerks on the two sides and possibly the ankle-jerks. The abdom inals were brisk and the plantars flexor. No sensory changes werepresen t. The blood pressure measured 130/75. T he spinal fluid showed less tha n1 cell per cm m . and 20 mg. protein : a negative Lange curve and W .R. X-rays of thechest and cervical spine showed no abnormality. At autopsy, the bulbar nuclei weredegenerated. N o evidence of pyram idal disease was found.It is suggested that in this case the nuclear degeneration may haveproduced a secondary effect upon intact suprasegmental mechanisms.Of 48 cases of bulbar palsy due to motor neurone disease examinedby Ragner Muller (1952), 16 had outbursts of laughter or weeping.Only 3 were witho ut clinical signs of bilateral pyram idal disease. N opatient in his series had signs of psychological disorder.It seems that although disorders of laughter are common in pseudo-bulbar cases with bilateral lesions in the hemispheres, they may occur

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5 9 6 REDVERS IRONSIDEwhen th e lesions are confined to the bu lb. I have observed a case ofuncontrollable laughter spells in a case of dhordoma attached to theposterior clivus which at autopsy was found to have compressed the ponsand me dulla chiefly, an d to a lesser extent th e crura cerebri. A slight degreeof hydrocephalus was present in this case.I find a difficulty in describing abnormalities of laughter apart fromthe accompanying emotional feeling, for the disintegration producedby disease may cause alteration, not only in the expression of feeling, butin the feeling itself. Patients will say " I can no t keep a straight face.Ho we ver mu ch I try, I cannot stop giggling. If I didn 't laugh , I sho uldcry ." Spasm s of giggling or loud laughter are often bro ug ht on byattem pts to talk, by excitement or em otion of any kind. The attem pt toconceal these gusts of inappropriate laughter which cause patients socialem barrassm ent, keeps them in a state of continual tension. They b urytheir faces in their hands in an effort to hide it, they are distressed, notam used. Th e following patient illustrated this. Th e clinical picture re-sembled that of pseudo-bulbar palsy due to arteriosclerosis, but the lesionwas a tumour.

Case 2. Unc ontrollable chuckling on attempting to talk with euphoria in a patientshowing bulbar speech, dyphasia, right homonym ous hemianopia and right-sided extensorplantar response. Mild confusion.T. M., aged 44, a right-handed m an, had complained of headaches for nine months .His speech became slurred, he began to talk in short phrases and to chuckle uncon-trollably when he tried to talk. He stated th at he was unable to control this chuckling.He seemed exaggeratedly happy, showing no evidences of anxiety or mental distress,althou gh he suffered from severe headaches and w as prone to almost d ailyfallingattacksin which he fell limply to the ground without apparent loss of consciousness, incon-tinence or tongue-biting. At times both legs would jerk uncontrollably. All this wasin the early stages of his illness.On examination.He was euphoric and talked with difficulty owing to dysphasia,slurring dysarthria an d uncon trollable chuckling. He was mildly confused a nd elated.There was blurring of the m edial margin of the left op tic disc. The fields of visionshowed a complete right homonymous h emianopia to the mid-line. The jaw-jerk wasincreased. An u pper m otor neurone type of facial weakness existed on the right sideand the right plantar respo nse was of the extensor type. The abdominal reflexes werebrisk, uppe r and lower, and there were no abnorma l motor or sensory signs. Th eblood pressure measured 115/80. X-rays of the skull showed marked pressure atro phyof the sella. He became restless and excited and then stuporose, and a week afteradmission to hospital died, in spite of tapping of the lateral ventricles.

This patient showed exaggerated laughter precipitated by attemptsat talking, with dysph asia, euph oria and mild confusion. H is disord erof laughter was therefore complex; involuntary laughter was accom-pan ied by disturban ces of em otional feeling. Speech disorder and in-tellectual insufficiency were also present.At autopsy a glioblastoma occupied the hypothalamus, reaching the surface at thetuber cinereum w hich it displaced dow nwards. In the left hemisphere there was tumour-

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DISORDERS OF LAUGHTER 597spread from the mid-line to involve the thalamus, globus pallidus, and part of theputamen, reaching up as far as the caudate nucleus and impinging on the lateralventricle, into which there had been bleeding. There was a discrete and apparentlyunrelated area of softening in the subcortical white matter of the left anterior frontalpole, the size of a sixpenny piece. No dilatation of the lateral ventricles existed.

In pseudo-bulbar cases the pathological emotionalism does not neces-sarily persist. If the patient improves and regains volitional control, theemotionalism lessens or disappears. Curiously it may disappear after afurther ictus.(2) Fits of Laughter as an Epileptic Phenomenon

It has long been known (Trousseau, 1873) that bursts of laughteror giggling may constitute an epileptic fit or its aura. The patient isusually, but not invariably, unaware that he has laughed when the attackis over. In F6r6's (1898) case, attacks were preceded by loquacity andlaughter. In Frigerio's (1899) patient, the laughter was intermingled withbabbling speech. Wilder's (1931) case saw fortification spectra and ex-perienced an odour of burning in the attacks, and in the cases of Mills(1912) and Rogal (1937) automatism occurred. The close resemblance ofthese cases to so-called uncinate or temporal lobe epilepsy is most striking.Incidentally one may remark how these attacks are sometimes attributedto rudeness, hysteria, compulsions of an obsessional kind, early schizo-phrenia or migraine.

Case 3. Psychom otor attacks with "deja vu" feelings and outbursts of laughter,probably epileptic, in a young man aged 18 years.C. H., aged 18 years, who is left-handed, has complained of strang e feelings for twoyears. In the attacks he has a sense of familiarity with situations"As if it has allhappened before. Something passes across my mind which has been there before.It is like trying to remember a dream. I can remember what I was thinking and doingin previous attacks, but the memory goes as soon as I recover."He thinks that his attacks are sometimes brought on when he is near bright orflickering lights, and he described one attack in a cinema. He says he does not realizethat he has laughed or has had one of his attacks until some hours afterwards, whenhe manages to remember it. During the attacks he is unable to talk to people.In add ition to these attacks he describes sensory symptoms in which he has teichopsiawith spreading numbness in the gums and teeth, the arm and leg, usually, but notalways, on the left side. His attacks come about once a week. In on e he said he feltcold in the stomach, laughed slightly and felt weak and dazed. Occasionally he hasto hold on to things to prevent falling. He thinks that some of his attacks are broughton by being in an em barrassing situation, or when he sees somebody being made a foolof. He does not seem to lose consciousness completely, buthas a feeling of recurrenceof thoughts that he has had before.Neurological examination showed no abnormality. Straight X-rays of the headwere norm al. Several EEG examinations were made, all of them suggesting thediagnosis of idiopathic epilepsy. In one of these examinations a focus was present in

the right temporal region, probably not structural.His attacks are not much influenced by anti-convulsants.

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5 9 8 REDVERS IRONSIDECase 4.Explosive laughter and giggling as an epileptic manifestation in a childaged 8 years.Patricia M., aged 8 years, was recently in the Maida Vale Hospital under the careof Sir Russell Brain. Soon after birth she had begun to have two to twelve attacks of

laughter durin g the day mostly, bu t also in sleep. The attack s came on explosivelyand suddenly; she either giggled or laughed heartily and then appeared vacant or dis-tressed. Her hands would clench,her arms would shake and her elbows flex. The rightcorner of her mouth would draw up and in some of the attacks she would be incon-tinent of urine or would drop things.The EEG was abnormal and showed a generalized dysrhythmia without any specialfocus in the tempora l lobe. She ha d no focal neurological signs. After she was puton anti-convulsants she began to have fewer and less marked attacks.Roubicek has described personal cases and reviewed the literature(1946).C. K. Mills (1912) described the case of a young man aged 29 years wh o had sufferedfrom episodic seizures in infancy. A t the age of 19 years he began to have attacks ofsmiling with disturbance of consciousness and twitchings of the left side of the face.At the age of 25 years he had Jacksonian attacks affecting chiefly the left face andupper limb preceded by a high-pitched cackling laugh, then vacancy, then automaticwalking. The right frontal lobe was explored by C. H . Frazier and a cond ition re-sembling cortical atrophy was found.I am indebted to Professors Dott and Cappell who allow me to quotethe following case, first published by Dott (1938) and referred to byPurdon M artin (1950). The tumour was an astrocytoma of the floorof the third ventricle, whose attachment was restricted to the region of themammillary bodies. The nuclei of the hypothalamus and th e tumourrelationships to surrounding structures have now been most meticulouslyidentified by Professor Cappell. This work formed one of the demon-strations at the recent Second International Congress of Neuropathology.This small girl had fits almost from birth. Delivery had been prolonged, w ithdifficulty in establishing b reathing after birth. The character of her fits soon began tochange and at the age of 3 her father distinguished short outbursts of giggling andlaughing, often preceded by an aura of preoccup ation. Th e severe fits were of thegrand mal type.During her first years of life she developed signs of precocious pubertyvaginalbleeding, enlargement of the breasts and other secondary sexual characteristics. A tthe age of 4 she had innumerable laughing itsduring waking and sleeping hou rs. Inmany attacks a crescendo of laughter terminated in loss of consciousness with to nic fits.She was shy and m odest for her age. Ab out the age of 4 years she was destructiveand m alicious. Between 4 and 8 years she spoke little. Thro ugh out h er life she showeda strange disorder of emotion. She was indifferent to her family an d others except a girlneighbour nine years older, to whom she was passionately attached in a jealous andpossessive fashion. A part from this, her lack of emo tional expression am ountedalmost to emotional pa ralysis. Precocious pube rty, emo tional disorder with fits andfits of laughter constituted the only signs of central disorder.The autopsy findings weie as follows: the tumour, whose attachment was restricted

to the mam millary bodies, was large, 4 x 3-5 x 5-5 cm., and projected into the thirdventricle. Th ere were no evidences of increased intracranial pressure or hy drocepha lus.

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DISORDERS OF LAUGHTER 599Th e growth had flattened th e pons and cerebral peduncles and elevated the floor of th ethird ventricle which was not dilated. All the hypothalam ic nuclei could be identifiedmicroscopically.

The case is important evidence of the hypothalamic origin of suchattacks. The literature was fully reviewed by Purdon M artin (1950),who quoted Gerard Lefebvre's (1939) case of probable hypophysealtumour, and described the autopsyfindings n a striking case of his own,who died soon after the onset of fits of laughter from rupture of a sac-cular basal aneurysm involving the corpora niammillaria. His patientdied from subarachnoid haemorrhage. Purdon Martin considered that theapparent mirth in such cases is "sham" and that the patient's emotionalstate in such an attack is not tha t of amusement or joy. The laughter mayor may not be remembered, it may be transient or prolonged, occurringduring sleep or in the waking state with or without disturbance of con-sciousness.The following case, that of a small girl aged 11 years, showed bouts ofspasmodic weeping cuhninating in unconsciousness and falling. A basalgliomafilled he interpeduncular space and involved the upper part of thepons. The case was published by Purves-Stewart and was once undermy care.

Case 5. Attacks of explosive uncontrollable weeping culminating in unconsciousnessIn a girl aged 11 years, with chiasmal blindness.A. B., a small girl, aged 11 years, began to have occasional causeless vomiting.This was followed six weeks before admission by uncontrollable attacks of weepingculminating in unconsciousness. In these attacks she fell down with clenched fists, buther knees were said to crumple up und er her. Before these attacks she complainedof being unable to see clearly and her face was flushed.She was admitted to hospital as a case of hysteria, but it was clear that she was blind,although the op tic discs and fundi were norm al. Th e pupils, widely dilated, wereinactive to light, at times the left was larger than the right. The arm-jerks and theknee- and ankle-jerks were absent. Th e abdom inal reflexes were feeble, the leftlower abdom inal was absent. Both plan tars were flexor. Kernig's sign was positive.Several convulsive attacks occurred before d eath two to three weeks later. Thepatient had developed a right oculomotor paralysis and bilateral extensor plantarresponses.At autopsy a basal glioma was found in the interpeduncular space infiltrating theupper pa rt of the pons, the third nerve and the optic chiasma. The tumour had ex-tended inwards between the corpora quadrigemina and the iter and both lateralventricles were dilated.

A relationship undoubtedly exists between natural laughter, alterationsin muscle tonus , and states of sleep or stupor. All may be observed inotherwise norm al persons as well as in disease of the basal structures of thebrain. Fere (1898) reported a case where fits of laughter were followedby an irresistible desire to sleep.True narcolepsy with cataplectic attacks in which emotional disturbance,especially laughter, results in toneless collapse without loss of conscious-

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6 0 0 REDVERS IRONSIDEness, may be due to some diffuse disease or injury to the hypothalamicareas. Laughter of the normal hearty kind may precipitate fits inepileptically predisposed individuals, and people with pathologicalnarcolepsy may develop epilepsy later in life.I have never myself known true narcolepsy conditioned by normallaughter to be associated with a brain rumour.

In other cases the laughter is prolonged and ends in hemiplegia, a fit,stupor o r demen tia. This has been called " Ictus ridenti."Cases of prolonged laughter followed by hemiplegia, stupor or dementia(ictus ridenti) are here considered in the epileptic gro up . Th e laug hterspell in such cases m ay last ho ur s, or as long as weeks. M an y bu t no t allhave cerebral arteriosclerosis. Fere (1903) called this phe nom eno n "L efou lire prodromique."One of Fere's two cases was that of an adv ocate, aged 64 years, a grave,serious and reserved person. He began having bursts of unco ntrollablelaugh ter, the mo re severe ones being followed by an irresistible desire forsleep. Four months later, consequent upon a laughter spell, he developeda left hemiplegia and survived for eighteen months after the attack, some-what demented. The hemiplegia put an end to his attacks of laughter.This is no t always so . A subsequ ent ictus ma y cause recurrence of bo utsof laughter after a period during which emotional stability has been re-gained. In And ersen's case (1936) the autopsy showed that intracerebraland ventricular haemorrhage from a penetrating branch of the posteriorcerebral artery caused death. After sudd en epileptic laugh ter with upw arddeviation of the eyes which lasted for an hour and a half, the patient, aknown pseudo-bulbar case, developed not hemiplegia but coma and diedin twenty-four ho urs. Post-mo rtem exam ination of the brain showedsoftenings in bo th hem ispheres. Rec ent intracere bral haemorrhage haddestroyed b oth intern al capsules an d filled the third ven tricle. Bo ththala m i were partly involved in the de struction . The blood filling thethird ventricle had spread down the iter into the fourth. There was nosubarachnoid hasmorrhage. Badt's (1927) case showed bilateral thalamichaemorrhage.In the case of Meige and Behague (1919) the patient had had craniotom yfor a large traumatic subdural haematoma following head injury due toshrapnel. There had been dural pen etration. Long spells of laughter(one lasted fifteen days) eventually gave way to attacks of laughter withloss of consciousness and convulsions.The long duration of the laughter in these cases seems to be related toactive destruction of brain tissue by a gradually increasing haemorrhage.The following personal case illustrates "Le fou rire prodromique."

Case 6. Mrs. E. C , aged 58, had five years previously had a stroke, after which shedragged the right foot. Two years later she had ano ther more severe stroke which

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DISORDERS OF LAUGHTER 601affected the left side, and after this she lived only a bathchair existence, although shecould walk with little steps unaided.One evening she had a sudden giddy attack, in which she fell to the floor. Shemanaged to get into her bed without help. She then commenced to laugh and con-tinued to laugh continuously for three hours, becoming more and more exhausted.At the end of this period she passed into a stupor lasting eighteen hours. After sheregained consciousness she was found to have a severe right hemiplegia with dysphasiaand she was doubly incontinent with mild dementia and bilateral extensor plantarresponses. Du ring the last three years of her life, following upon this attack, she usedto laugh immoderately at trivial causes.(3) Disorders of Laughter Consequent upon Excitement, Euphoria andOther Mental Changes

States of excitement (or apathy) due to discrete brain lesions maycause laughter, hilariousness, and an excessive feeling of well-being.Such symptoms have long been known to follow lesions of the orbitalpa rt of the frontal lobe. Diffuse c erebral intoxica tions or anoxia as wellas psychotic states cause similar symp tom s. M an y of the recorded casesare tumours involving the hypothalamus or its connexions.One of the earliest cases recorded is that of Bruce (1883), where apatient with a temporal lobe tumour suffered from fits of excitement withlaughing and crying. His patient became dysphasic.Van der Horst (1953) described a case of slow-growing glioma of theleft temporal lobe which gradually over a period of years destroyed mostof the limbic lobe and hyp othalam us. This case at one stage had boutsof excitement in which he made speeches in jargon language with violentrhetorical expressive gestures. As the fit cam e to an end after threeminutes his voice would sink to diminuendo and a smile would spreadover his face. His recollection of these attacks w as im perfect.Lesions of the third ventricle and hypothalamus as well as corticallesions may be associated with symptoms resembling psychosis or demen-tia particularly states of stup or. This was described by Ca irns (1952) inchildren. Occasionally, how ever, in hyp othala m ic lesions episodic statesof excitement with laughter occur with hilarious or obscene talk, usuallyas a prelude to stupo r with dem entia or death . Th e subject has been fullydealt with by Cox (1937), who described h ypothalam ic tumo urs and otherbasal lesions producing exalted states of consciousness with excitement.The phenomena resemble those of psychomotor epilepsy, but terminatein confusion o r dem entia. Fo erster and G agel (1933) had noted d isturb -ances of this kind whilst operating upon patients under local anaesthesia.One patient (Case 3), operated upon for a craniopharyngioma, was lyingquietly up on the table until piecemeal remov al of his tum ou r was attempted.He then began to talk incessantly, made jokes, witty remarks, gesticulatedwith his hand s and feet and m ade qu otatio ns in Greek, La tin and Hebrew .H e gradually became m ore and m ore incoherent. After the operation hewas demented and confused. Hyp erpyrexia occurred and he died.

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6 0 2 REDVERS IRONSIDETw o o ther cases described by them a re of interest. In Case 4 (papillomaof the choroid plexus) whilst they were swabbing blood from the thirdventricle, the patient became lively and talkative, jokin g an d whistling.This type of response seemed to be obtained by touching the infundibularregion. After operation the patien t became confused and died withhyperpyrex ia. In their Case 5, touchin g the infundibular region caused t h epatient t o becom e excited and sing. Schuster (1902) (quoted by Cox) h adpreviously described excitement with diencephalic tumours.Percival Bailey (1948) described attacks of laughing and weeping withexcitement, sleeplessness and pyrexia in a boy aged 13 years during therecovery pha se after removal of a third ventricle tum ou r. Th e patie ntregained his em otional con trol within three weeks and m ade a satisfactorygeneral recovery.In Cushing's (1912, "The Pituitary Body and its Disorders") Case 17, a largeinterpeduncular growth in a man aged 35 years was associated with emotional ch ange s:he was over-hilarious or lachrymose by turns, loquacious and irrelevant, irritable andforgetful, but not disoriented.At autopsy, the tumour, an infundibular "teratoma" can be seen in the photograph-to have elevated the floor of the third ventricle, widening the interpeduncular space,flattening the pons and elongating the mid-brain. The floor of the third ventricle, th emammillary bodies and the pituitary were compressed but intact. There was mo derate'hydrocephalus.Deep indentation of the under surfaces of both temporal lobes was observed in thiscase. It seems likely that this caused damage to cortico-bulbar tracts.Davison and Kelman's (1939) Case 32, showed at post-mortem a left-sided menin-gioma lying near the mid-line, invading and destroying the left portion of the hypo-thalamus, the lateral thalamic nuclei, globus pallidus, subthalamic body, cerebralpeduncle and mesencephalon.He had recurrent spells of stupor with spastic right hemiparesis and right-sidedhypalgesia. His appearance was Parkinsonian. The right pupil was larger than th eleft and there was weakness of elevation and depression of the eyes. Lateral gaze wasimpaired to both sides with nystagmoid jerks.Between bouts of stupor he laughed or cried involuntarily, without feelings of sad-ness or happiness. He was rather lethargic, but not dysphasic. The right planta rresponse was extensor.Here emotional expression was dissociated from feeling in his spells of laughing and

crying. There was notable destruction of part of the mesencephalon as well asdiencephalic invasion. The association of emotional apa thy in this case is of interest.The line of distinction between such cases and epileptic discharges is hard to define.In euphoria an excessive feeling of well-being is expressed positively byfrequent laughter, not spasmodic, and negatively by the absence ofanxiety or men tal uneasiness. Th e condition is less com mo n than w asbelieved in adv ance d mu ltiple sclerosis. In such cases lesions in b o thhemispheres are presen t, involving cortico-hy pothalam ic tracts . T hecondition recalls "anosognosia" where the patient will not admit theexistence of his hemiplegia or other gross neurological lesion.In hyperpathia found in thalamic hemiplegia with disease of the ventral

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DISORDERS OF LAUGHTER 6 0 3postero-lateral nucleus of the thalamus an excessively pleasant emotionalquality is imparted to the perception of peripheral sensations.In the "Witzelsucht" of rare cases of frontal tumour, pathologicaljoking and punning exist with emotional blunting and lack of socialrestraint. Such cases are vastly amused by their own jok es, which do no tusually am use others. Facile laughter consequ ent up on em otionalliability is found in cases with defective memory and attention, or defectsin perception of time and space due to gross disease of the cortex orcortico-hypothalamic tracts.

DISORDERS OF SMILINGParalysis of the emotional and expressive movements of the face occurswithout corresponding disturbance of voluntary facial movements whencarrying out definite tests at command, such as showing the teeth orwhistling. This is referred to as "H yp om im ia" or "m imic paralysis ."In such cases there is no disorder of em otional feeling, nor release of thelaughter mechan ism.There are many fallacies associated with the identification of thisphysical sign. It may occur as a personal peculiarity without kno wnphysical lesion. It may be simulated by unilateral Parkinson ism produ cingrigidity, or by unilateral cerebellar disease producing hypotonia of thefacial muscles on one side. Th e usual explanation is th at it is du e toinvolvement of "psycho-bulbar tracts" connected with facial emotionalexpression.It is found characteristically in deep centrally placed lesions of thecontralateral tem poral and frontal lobes. Its mechanism is obscu re. W eknow that in hemiplegia an affected muscle may be paralysed for onefunction an d not for an oth er. Th e same may be tru e for the facial mu scleswhich are under both pyramidal and extrapyramidal control . In norm alsmiling there is innervation of certain muscles and relaxation of others,i.e., there is reciprocal innerva tion. In temp oral or frontal lesions thefacial muscles m ay be paralysed for one function p redom inantly. Th e

converse m ay be seen after hem ispherectom y, where lower facial we ak-ness of volun tary m ovem ent is accom panied by a smile which is freeand equal on the two sides.Some cases of Parkinsonism with paralysis of facial expression complaintha t they are unable to laugh or to enjoy a jok e as they did before th eonset of their illness.

DISCUSSIONNone of the foregoing observations can be held to refute the commonlyaccepted view that pathological laughter disorder is most frequent indisease of both hemispheres interfering with cortico-hypothalamic andcortico-bulbar tracts (voluntary and involuntary) controlling facio-respiratory mechanisms.

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6 0 4 . REDVERS IRONSIDEIn cases recorded of laughter disorder occurring with single hemiplegiait is exceedingly difficult to exclude the presence of pathological changesin the sound h emisphere. Autopsies on cases are few and p oorly do cu-

mented.Laughter disorder does not appear until after a second ictus in thesound hem isphere. A further ictus ma y, in some unexplained way,cause either disappe aranc e of the laugh ter or its recurren ce. Th e frequencyof laughter disorder in the pseudo-bulbar types of cerebral arteriosclerosismay pe rhap s be related not only to the b ilateral distribution of the lesions,bu t also to their frequent d istribution in the basal ganglia. In cases withlaughter disturbance who survive, a measure of control is regained andthe disability becomes much less evident.In uncomplicated bulbar palsy due to motor neurone disease laughterdisorder m ay oc cur. It may be impossible in certain cases to find clinicalor pathological evidences of pyramidal disease, although the motornuclei of the bulb sh ow evidence of dam age . Of 8 cases of bulbar p alsywith disordered laughter, I found 3 showing no pyramidal signs, and 1with no pathological evidences of pyramidal disease, although the bulbarnuclei were partially destroyed.It has been stated th at laughter disorders do not result from pathologicallesions situated below the hyp othalam ic or mid-b rain level. I haveproduced evidence that this is a fallacy.Single lesions, if appropriately placed, also cause pathological laughter.Notewo rthy in my cases, as in Purdon M artin's and D avison and Kelm an's,is the frequency of mid-line lesions, especially tho se involving th e p osteriorhypothalamus and mid-brain.Th e ro le of the hyp otha lam us has n ot, in my view, received sufficientattention. Fo r the produc tion of an emotional response, whether oflaughter or of weeping, some degree of integrity of the hypothalamicnuclei seems to be essential. W hen these nuclei or the co rtico-hypo thalamictracts are destroyed, emotional deadness and apathy are much more inevidence than hilarity and excitement.Lesions of the posterior hypothalamus seem to cause a pathologicallaughter which is secondary to excitement of the em otions. W hen thereis also excited manic talk, cortical mechanisms must also be stimulated.M any of the hypo thalam ic lesions are large and expand laterally. Theymay be seen to cause a deep guttering of the medial aspects of bothtem pora l lobes. Such indentations ma y interfere with cortico-bulbarfibres controlling the facio-respiratory mechanisms in the bulb.The classification as epileptic of more prolonged fits of laughter,followed by hem iplegia or stup or, seems justifiable o n the analog y of theJacksonian attack followed by paralysis, or of the epileptic motor aurafollowed by unco nscious ness. They generally occur during progressivebrain destruction by a haemorrhage.

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DISORDERS OF LAUGHTER 6 0 5Temporal lobe attacks with laughter.The association of laughterwith speech disturbance and excitement in rare cases of attacks ofepilepsy of the temp ora l lobe type is of great interest. It is well know n

that psycho-sensory attacks are often accompanied by inappropriateemotional feelings of well-being, anger, misery, fear, unreality excitement.Motor accompaniments are observed adapted to such feelings, suchas running or violence. Laug hter or weeping, excited speech, jarg ontalk , in such fits m ay have a similar exp lana tion. Th e idea is gainingground that the temporal lobes (possibly the limbic structures especially)are important in the elaboration of emotional feelings and states ofem otion al experience. It m ay be recalled tha t Penfield (1950) observedthat electrical stimulation of the temporal lobe in the conscious patientcaused the recollection of past experiences of a whole chain of events,with an altered affective tone.An analysis of these cases suggests that abnormal laughter responsescan be produced by lesions at various neurological levels including thebulb . The wide distribution of the lesions is noteworthy.THEORETICAL

The increase in our knowledge of the central architecture of the auto-nomic system is one of the most striking modern advances in anatomyand physiology . In the earliest years of th e centu ry the central originof the cervical sympathetic was represented on anatomical diagrams by ablo b in the region of the med ulla. Later the hyp othalam us (somew hatconservatively described as the "head ganglion" of the autonomic system)was adde d. No wa day s, following on the wo rk of Ra nso n (1934) and LeGros Clark (1938), it is clear that we must superimpose other structuresupon our diagrams of the hypothalamus, particularly the limbic structuresand certain upward tracts to the orbital cortex, and downward tractsto the reticular formation a nd the bu lb. Some of these tracts activate,othe rs inhib it. Systems of fibre trac ts may exist within the brain in a stateof balance or equilibrium similar to that which exists between the sym-pathetic and parasympathetic.The "limbic" lobe was so called by Broca (1878) because it forms theme dial "lim bu s" or limit of the general cavity of the hemisphere. On eof the earliest comparative anatomists to link the hypothalamus with thelimbic structures was G. Elliot Smith (1919). He suggested that the cortex,which is developed in association with the olfactory apparatus and thehypothalamus, provides a system for integrating an animal's varioussensory impressions and imparting to them the quality of emotion.Many neurologists on the basis of study of lesions of the temporal lobeand temporal lobe epilepsy hold the view that structures in the temporallobe are important in the development of emotional feelings and ex-periences.

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6 0 6 REDV ERS IRONSIDEDownward tracts from the hypothalamus, medullated and non-medullated, appear to end in the reticular formation of the bulb. Theymay be important in regulation of respiration and other autonomic

activities. It is suggested tha t facio-bulbar automatisms of laughter a remediated by such tracts and that they are the "final common pathway"for laughter.Schaltenbrand and Girndt (1925) and Bard (1934) have shown that"sham rage" in animals can be demonstrated in various diencephalicpreparations. In mid-brain decerebrate preparations the typical reactionis said to be more modified, partia l and transient. The placid activityof such a prepared animal belies its ferocious appearance. These reactionshave been called "pseudo-affective." In these preparations em otionalfeeling was judged by the animal's behaviour to be absent or dispropor-tionate to its appearance. It was on this analogy that Purdon M artintermed attacks of mirthless laughter in disease states, "sham laughter,"an apt comparison."W hat experimental physiologists have produced from diencephalicstimulation is in some ways similar to what is seen in disease, i.e. positiveor negative fragments of a total response. By stimulation or by destructionthey have produced grimaces, respiratory arrhythmia, phonation; or onthe other hand akinetic mutism or poverty of movement.Neurologists and neurosurgeons have contributed most to our know-ledge of laughter and weeping. Neurologists, by their studies of focallesions and psycho-sensory epilepsy, have shown the relation of laughter,weeping or emotional states to the hypothalamus, the temporal lobesand their connexions. Neurosurgeons have demonstrated that stimulationof the posterior hypothalamus caused excited behaviour with laughterand manic flow of talk.The mechanistic theory of m otor pathways proposed by W ilson is amost useful practical concept, but, as he himself admitted, it is nota complete explanation. Samson W right (1952) modified it to includethe hypothalamus, in his diagram of the efferent pathways for emotionalexpression. Still, in my view, no complete explanation can be given.I am not proposing to advance the view that the hypothalamus is alaughter centre. Norm al laughter has affinities with speech and mentalprocesses. I think the effects of stimulation or destruction of hypothala-mic structures are more likely to be due to their connexions with otherparts of the brain. Euphoria and smiling may have to do with upwarddischarges from the hypothalamus, and the low-level dissociated bulbarand respiratory automatisms of laughter with downward discharges fromthat area.These responses, however, normally seem to be subordinate to thewill and under the domination of both hemispheres. They may be activatedreflexly by psychical or peripheral afferent stimuli.

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DISORDERS OF LAUGHTER 6 0 7Of natural emotional states, Hughlings Jackson (1931) said: "I believethere is a duplex condition in emotional states, negative (loss of control),and positive (overaction of lower centres)."In a normal emotional response in man involving laughter, we maysay that there is a sensory phase, a mental phase involving psychologicalprocesses such as cognition, conation when we "see a jo ke " or "hav eour sense of hu m ou r tickled." Finally there is the mo tor or expressiveph ase. Th e new cortex as well as the old cortex of the limbic lobe playsits pa rt in em otion al reaction s. These manifestations of feeling haveaffinities with speech and gesture and partake of the neurological com-plexities of both . There is a languag e of feeling as well as of thou gh t,but it is at a sub ord inate level of integr ation. In this sub ordin ationnot one but both hemispheres seem to participate.W hen we consider abn orm al laughter responses we may say thatlesions in widespread areas of the brain cause abnormal emotionalactivity at various levels.(1) At the lowest levelas at the highestinvoluntary, uncontrol-lable spasms of laughter or weeping occur which do not conform indegree or duration to emotional feeling and in which an appropriatestimulus may be lacking. They commonly cause embarrassment and dis-tress to the patient. M ental changes and disturbances of consciousnessare absen t. These occur in patients with lesions of the facio-respiratorybulbar nuclei and suprasegmental motor tracts. The majority but not allshow signs of bilateral pyramidal disease.(2) At th e interm ediate (p osterior diencepha lic and limbic level) aconvulsion of laughter analogous to Jacksonian epilepsy may occur withor without disturbances of consciousness. Laug hter may constitute theprodrome of an attack or the attack itself. These attacks often resembletemporal lobe fits. Sudden hypotonia may induce falling.(3) At the highest level (anterior hyp otha lam ic, frontal, tem pora l)emotional lability or emotional incontinence is part of a complexmental disorder shown by excited speech or behaviour and giggling.

Some mental functions may be stimu lated, others paralysed. Here theremay be coexistent deficits of m em ory, attentio n and perce ption. Largelesions situated n ear th e mid-line cause disturba nces at this level. Th eremay be associated dysphasia, dyspraxia, hemiplegia or visual field defects.These levels, how ever, are no t clearly defined clinically. In cere brallocalization it is not the emotional disorder, but rather the associatedsomatic findings which indicate the site of the lesion.

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